Qilong Capsule Alleviated MPTP-Induced Neuronal Defects by Inhibiting Apoptosis, Regulating Autophagy in Zebrafish Embryo Model
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Updated: Aug 13, 2025

Methylnitrosourea MNU-induced Retinal Degeneration and Regeneration in the Zebrafish: Histological and Functional Characteristics
Published on: October 20, 2014
Cailian Mo1, Shenghua Lin1, Zhen Li2
1Biology Institute, Qilu University of Technology (Shandong Academy of Sciences), Jingshidong Road No. 28789, Licheng District, Jinan, 250103, Shandong, China.
Abstract:
Qilong capsule (QLC) originates from the famous "Buyang Huanwu decoction" prescription. It is representative of drugs used in China during recovery from stroke, but its neuroprotective mechanism of action remains obscure. HPLC was used to evaluate the similarity of 10 batches of QLC samples. Then we used a zebrafish model to study the neuroprotective effect of QLC. At 24 hpf, embryos were treated with QLC and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and zebrafish were observed the neuronal length and the number of apoptotic cells in the brain at 72 hpf. At 120 hpf, we conduct zebrafish behavioural tests. We then also used qPCR to detect the expression of genes related to autophagy and apoptosis. The results showed that QLC significantly reduced the damage of dopaminergic neurons, the number of apoptotic cells in the brain, and alleviated motor disturbances induced by MPTP. We found that the mechanism of QLC activity involved decreased neuron cell death by inhibiting mitochondrial apoptosis and autophagy, promoting autophagy, degradation of alpha-synuclein, and neuron cell growth, and rescuing the function of neurons damaged by MPTP. The results indicated that QLC protected against MPTP-induced neuron injury and provided pharmacological evidence for clinical use of QLC.
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